scholarly journals Oral Kefir Grains Supplementation Improves Metabolism and Liver Antioxidant Enzymes Expression in Malnourished Mice

2020 ◽  
Author(s):  
Santos FR ◽  
◽  
Machado AS ◽  
Lelis DF ◽  
Guimaraes ALS ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Food Restriction ◽  
Control Group ◽  
Oral Supplementation ◽  
Hepatic Oxidative Stress ◽  
Novel Approach ◽  
Original Weight ◽  
Glucose Tolerance Tests ◽  
Kefir Grains

Scope: This study has a novel approach to investigate the effects of oral supplementation of kefir grains on metabolic improvement and the expression of the antioxidant enzymes Glutathione Peroxidase (GPx) and Catalase (CAT) of the liver in malnourished mice. Method and Results: Swiss mice were divided into four groups and subjected to two treatment phases: the food restriction phase of 20% in relation to the control group was maintained until animals reached a weight deficit of about 20% in relation to their original weight and the renutrition phase, the animals received diets every day for 30 days. Diets (chow powder plus kefir grains) were administered orally. Thereafter, during throughout the experiment measurements of body weight and energy consumption were obtained. After the end of treatment, fasting glucose tolerance tests were performed at night and insulin sensitivity with fed mice. Soon in then, the mice were euthanized by beheading in guillotine and the blood and liver were collected for evaluation of biochemical parameters, Histopathological assessments and Reverse transcriptase (RT-PCR). Conclusion: The present study demonstrated the kefir grains ability to modulate inflammation and hepatic oxidative-stress under malnourished-state. Keywords: Food Restriction; Malnutrition; Hepatic; Oxidative Stress; Nutrition

Alteration in the oxidative status of Drosophila melanogaster Meigen (Diptera: Drosophilidae) fed with a diet containing Centaurea depressa M. Bieb. (Asteraceae)

2020 ◽  
Vol 70 (2) ◽  
pp. 227-237
Author(s):  
Eda Güneş
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Total Protein ◽  
Protein Carbonyl ◽  
Control Group ◽  
Carbonyl Content ◽  
Protein Carbonyl Content ◽  
Freeze Dried ◽  
Dried Extract

Abstract The aim of the this study was to evaluate the effects of fresh, dried and freeze-dried Centaurea depressa M. Bieb. (Asteraceae) on the oxidant and antioxidant status of the model organism D. melanogaster Meigen (Diptera: Drosophilidae) experimentally. The study was carried out from 2016 to 2019, and plant leaf extracts (0-50 mg/l) were added to insect standard artificial diets. The total protein, protein carbonyl content and glutathione-S-transferase, superoxide dismutase and catalase activities were quantified at the insect’s third larval stage. Our data showed that protein carbonyl content varied from 2.70 nmol/mg protein in the control group to 59.11 nmol/mg protein in the group fed with fresh leaf extract signifying induction of oxidative stress. All extracts increased the levels of all antioxidant enzymes and decreased the amounts of total protein. Meanwhile, the group fed with the freeze-dried extract showed no significant difference in the levels of total protein and protein carbonyl content except at the 50 mg/l concentration of the extract. Moreover, this group had superoxide dismutase and catalase activities 4 to 5 times higher than in the control group. In conclusion, induction of oxidative stress indicates that the fresh form of C. depressa leaves may have potential as a natural pesticide, whereas induction of endogenous antioxidant enzymes by the freeze-dried extract suggest its potential as an antioxidant.

scholarly journals The effects of acutely and subchronically applied DL-methionine on plasma oxidative stress markers and activity of acetylcholinesterase in rat cardiac tissue

2020 ◽  
Vol 77 (2) ◽  
pp. 165-173
Author(s):  
Zarko Micovic ◽  
Sanja Kostic ◽  
Slavica Mutavdzin ◽  
Aleksa Andrejevic ◽  
Aleksandra Stamenkovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Ache Activity ◽  
Cardiac Tissue ◽  
Heart Function ◽  
Antioxidant Defense System ◽  
Rat Plasma ◽  
Physiological Solution ◽  
Control Group ◽  
Subchronic Treatment

Background/Aim. Chronically induced hypermethioninemia leads to hyperhomocysteinemia which causes oxidative stress, atherogenesis, neurodegeneration and cancer. However, little is known about the acute and subchronic effects of DL-methionine (Met). The aim of study was to assess the effects of acutely and subchronically applied Met on oxidative stress parameters in rat plasma [enzymes: catalase (CAT), glutathione peroxidise (GPx), superoxide dismutase (SOD) and index of lipid peroxidation, malondialdehyde (MDA)], and acetylcholinesterase (AChE) activity in rat cardiac tissue. Methods. The enzymes activities, as well as MDA concentration were evaluated following acute (n = 8) and subchronic (n = 10) application of Met [i.p. 0.8 mmoL/kg body weight (b.w.) in a single dose in the acute overload or daily during three weeks in the subchronic overload]. The same was done in the control groups following application of physiological solution [i.p. 1 mL 0.9% NaCl (n = 8) in the acute overload and 0.1?0.2 mL 0.9% NaCl, daily during three weeks (n =10) in the subchronic overload]. Tested parameters were evaluated 60 minutes after application in acute experiments and after three weeks of treatment in subchronic experiments. Results. There were no difference in homocysteine values between the groups treated with Met for three weeks and the control group. Met administration significantly increased the activity of CAT and GPx after 1 h compared to the control group (p = 0.008 for both enzymes), whereas the activity of SOD and MDA concentrations were unchanged. Subchronically applied Met did not affect activity of antioxidant enzymes and MDA level. AChE activity did not show any change in rat cardiac tissue after 1 h, but it was significantly decreased after the subchronic treatment (p = 0.041). Conclusion. Results of present research indicate that Met differently affects estimated parameters during acute and subchronic application. In the acute treatment Met mobilizes the most part of antioxidant enzymes while during the subchronic treatment these changes seems to be lost. On the contrary, the acute Met overload was not sufficient to influence on the AChE activity, while longer duration of Met loading diminished function of the enzyme. These findings point out that methionine can interfere with antioxidant defense system and cholinergic control of the heart function.

Butylated hydroxyanisole alleviates ferric nitrilotriacetate induced nephrotoxicity in rats by abrogation of oxidative stress

2013 ◽  
Vol 3 (2) ◽  
pp. 65-70
Author(s):  
Sabah Ansar ◽  
Mohammad Iqbal ◽  
Noura Al Jameil
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Antioxidant Enzymes ◽  
Control Group ◽  
Butylated Hydroxyanisole ◽  
Chemopreventive Agent ◽  
Microsomal Lipid Peroxidation ◽  
Hydrogen Peroxide Generation

In this study the effect of butylated hydroxyanisole (BHA), a phenolic antioxidantused in food on Ferric‐Nitrilotriacetate (Fe–NTA) induced nephrotoxicity is reported. Fe‐NTA (9 mg Fe/kg body weight, intraperitoneally) treatment enhanced the renal microsomal lipid peroxidation and hydrogen peroxide generation to ~2‐2.5 folds compared to saline‐treated control and glutathione levels and the activities of antioxidant enzymes decreased to a range of 2–2.5 fold in kidney. These changes were reversed significantly in animals receiving a pretreatment of BHA. Pretreatment with BHA prior to Fe‐ NTA treatment reduced microsomal lipid peroxidation and hydrogen peroxide generation to 1.3‐1.5 fold compared to control group and glutathione and the activities of antioxidant enzymes increased to a range of 1.5‐2 folds in kidney. Fe‐NTA administration enhanced value of blood urea nitrogen and creatinine to 3.7 and 2.5 fold respectively as compared to their corresponding control group. Administration of Fe‐NTA to rats receiving a pretreatment of BHA led to a significant diminution in both of these values. The results indicate that BHA is a potent chemopreventive agent and suppresses Fe‐NTA induced nephrotoxicity in rats.

scholarly journals The protective role of CsNPs and CurNPs against DNA damage, oxidative stress, and histopathological and immunohistochemical alterations induced by hydroxyapatite nanoparticles in male rat kidney

2019 ◽  
Vol 8 (5) ◽  
pp. 741-753 ◽  
Author(s):  
Israa F. Mosa ◽  
Mokhtar I. Yousef ◽  
Maher Kamel ◽  
Osama F. Mosa ◽  
Yasser Helmy
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Biological Effects ◽  
Male Rats ◽  
Nuclear Antigen ◽  
Male Rat ◽  
Control Group ◽  
Renal Tubules ◽  
Hydroxyapatite Nanoparticles

Abstract Hydroxyapatite nanoparticles (HAP-NPs) are an inorganic component of natural bone and are mainly used in the tissue engineering field due to their bioactivity, osteoconductivity, biocompatibility, non-inflammatory, and non-toxicity properties. However, the current toxicity data for HAP-NPs regarding human health are limited, and only a few results from basic studies have been published. Therefore, the present study was designed to investigate the beneficial role of chitosan nanoparticles (CsNPs) and curcumin nanoparticles (CurNPs) in alleviating nephrotoxicity induced by HAP-NPs in male rats. The results showed that HAP-NPs caused a reduction in antioxidant enzymes and induced lipid peroxidation, nitric oxide production and DNA oxidation. Moreover, HAP-NP administration was associated with intense histologic changes in kidney architecture and immunoreactivity to proliferating cell nuclear antigen (PCNA). However, the presence of CsNPs and/or CurNPs along with HAP-NPs reduced the levels of oxidative stress through improving the activities of antioxidant enzymes. Also, the rats administered the nanoparticles showed a moderate improvement in glomerular damage which matched that of the control group and showed mild positive reactions to PCNA–ir in glomeruli and renal tubules in the cortical and medullary portions. These novel insights confirm that the presence of chitosan and curcumin in nanoforms has powerful biological effects with enhanced bioactivity and bioavailability phenomena compared to their microphase counterparts. Also, they were able to ameliorate the nephrotoxicity induced by HAP-NPs.

scholarly journals STREPTOZOTOCIN-INDUCED OXIDATIVE STRESS IN DIABETIC RATS - A DEFENSIVE EFFECT OF PSYDRAX DICOCCOS

2018 ◽  
Vol 11 (11) ◽  
pp. 378
Author(s):  
Ravi Kumar V ◽  
Sailaja Rao P
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Blood Glucose ◽  
Methanolic Extract ◽  
Antioxidant Effect ◽  
Control Group ◽  
Standard Drug ◽  
Antihyperglycemic Activity ◽  
Glucose Levels ◽  
Blood Glucose Levels

Objective: The present study was aimed to evaluate the antihyperglycemic activity and in vivo antioxidant effect of methanolic extract of whole plant of Psydrax dicoccos (MEPD) belonging to the family Rubiaceae.Methods: MEPD was prepared by Soxhlet extraction. Wistar rats weighing (180–200 g) were divided into six groups (n=6), with three doses of 100 mg/kg, 200 mg/kg, and 400 mg/kg of extract. Metformin was used as a standard drug. Diabetes was induced by streptozotocin (STZ) (40–50 mg/kg, i.p) in control group. The animals were treated with different doses of extracts for 21 days, and on the 22nd day, the blood glucose levels along with antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and lipid peroxidase (LPO) were determined.Results: The phytochemical screening of the extract showed the presence of carbohydrates, phenolics, flavonoids, glycosides, and tannins. The methanolic extract of MEPD at the dose of 200 mg/kg body weight showed a significant reduction in blood glucose levels (**p<0.001) with the value of 151.2 mg/dl on the 22nd day at 8 h. A promising antioxidant effect was also evident from the determination of antioxidant enzymes such as SOD, CAT, and LPO.Conclusion: The P. dicoccos extract revealed a potential effect of antihyperglycemic activity and combating nature on oxidative stress induced by STZ.

scholarly journals Weaning Induced Hepatic Oxidative Stress, Apoptosis, and Aminotransferases through MAPK Signaling Pathways in Piglets

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Zhen Luo ◽  
Wei Zhu ◽  
Qi Guo ◽  
Wenli Luo ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathways ◽  
Redox Status ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Control Group ◽  
Hepatic Oxidative Stress ◽  
Mitogen Activated Protein ◽  
D 20 ◽  
Mapk Signaling Pathways

This study investigated the effects of weaning on the hepatic redox status, apoptosis, function, and the mitogen-activated protein kinase (MAPK) signaling pathways during the first week after weaning in piglets. A total of 12 litters of piglets were weaned at d 21 and divided into the weaning group (WG) and the control group (CG). Six piglets from each group were slaughtered at d 0 (d 20, referred to weaning), d 1, d 4, and d 7 after weaning. Results showed that weaning significantly increased the concentrations of hepatic free radicals H2O2and NO, malondialdehyde (MDA), and 8-hydroxy-2′-deoxyguanosine (8-OHdG), while significantly decreasing the inhibitory hydroxyl ability (IHA) and glutathione peroxidase (GSH-Px), and altered the level of superoxide dismutase (SOD). The apoptosis results showed that weaning increased the concentrations of caspase-3, caspase-8, caspase-9 and the ratio of Bax/Bcl-2. In addition, aspartate aminotransferase transaminase (AST) and alanine aminotransferase (ALT) in liver homogenates increased after weaning. The phosphorylated JNK and ERK1/2 increased, while the activated p38 initially decreased and then increased. Our results suggested that weaning increased the hepatic oxidative stress and aminotransferases and initiated apoptosis, which may be related to the activated MAPK pathways in postweaning piglets.

scholarly journals The possibilities of pharmacological correction of ademol oxidative stress in rates with traumatic brain injury

2021 ◽  
Vol 25 (2) ◽  
pp. 192-195
Author(s):  
S. I. Semenenko
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Brain Injury ◽  
Oxidative Degradation ◽  
Male Rats ◽  
Control Group ◽  
Nacl Solution ◽  
Amantadine Sulfate

Annotation. An important measure of intensive care in patients with traumatic brain injury (TBI) is the use of pharmacotherapeutic agents with antioxidant properties. The aim of this study was to evaluate the effect of ademol compared with amantadine sulfate and 0.9% NaCl solution on the course of oxidative stress in the brain of TBI rats. The experiments were performed on 28 white male rats weighing 160-190 g. The experimental TBI model of severe severity was caused by the action of a carbon dioxide flow under pressure created using a gas balloon pneumatic gun. The therapeutic effect of ademol on model TBI was evaluated with a 2 mg/kg dose. The pseudoperated animals and control group received a 0.9% solution of NaCl and amantadine sulfate at a dose of 2 ml/kg and 5 mg/kg i/v. Data were processed using StatPlus 2009. We used the parametric criterion of t-Student, non-parametric criterion of W. White, paired criterion Ť. Wilcoxon, Fisher's angular transformation at p <0,05. In the course of the experiment, it was found that treatment of rats with TBI ademol leads to a decrease in the activity of lipid peroxidation and oxidative degradation of proteins (p<0.05) and promotes the normalization of the activity of antioxidant enzymes in cells of traumatically damaged brain (p<0.05). The use of ademol compared to amantadine sulfate and 0.9% NaCl solution was accompanied by a more significant decrease in the activity of lipid peroxidation and oxidative degradation of proteins and an improvement in the level of antioxidant enzymes in damaged brain of animals with TBI (p<0.05).

scholarly journals Antioxidant enzymes and fatty acid status in erythrocytes of Down syndrome patients

1998 ◽  
Vol 44 (5) ◽  
pp. 924-929 ◽  
Author(s):  
M-Cruz Pastor ◽  
Cristina Sierra ◽  
María Doladé ◽  
Elisabet Navarro ◽  
Nuria Brandi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Down Syndrome ◽  
Catalytic Activity ◽  
Antioxidant Enzymes ◽  
Chromosome 21 ◽  
Control Group ◽  
Acid Status ◽  
Antioxidant Mechanisms ◽  
Long Chain

Abstract The excess of genetic information in patients with Down syndrome (DS) produces an increase in the catalytic activity of superoxide dismutase (SOD1), an antioxidant enzyme coded on chromosome 21. It has been suggested that an increase in oxidative stress in DS patients may cause adverse effects in the cell membranes through the oxidation of polyunsaturated fatty acids (PUFAs). The aim of this study was to evaluate the cellular antioxidant system by determining the catalytic activity of the SOD1, glutathione peroxidase (GPx), catalase (CAT), and glutathione reductase (GR) enzymes and the concentrations of α-tocopherol in red blood cells (RBCs) in a group of 72 DS patients. The profile of fatty acids in the phospholipids of RBC membranes was also evaluated. The activity of the erythrocyte antioxidant enzymes is significantly higher in the DS group than in the control group (SOD1, 635 ± 70 U/g Hb vs 476 ± 67 U/g Hb; CAT, 1843 ± 250 U/g Hb vs 1482 ± 250 U/g Hb; GPx, 23.2 ± 5.3 U/g Hb vs 21.5 ± 3.6 U/g Hb; and GR, 9.32 ± 1.4 U/g Hb vs 6.9 ± 1.3 U/g Hb, respectively). No differences were observed in RBC α-tocopherol concentrations between the two groups studied. Long-chain n6 PUFA (C20:3n6, C20:4n6) concentrations were increased in DS patients, suggesting enhanced Δ-6-desaturase activity. The long-chain n3 PUFA (docosahexenoic acid) does not appear to be affected by increased oxidative stress, probably because of the existence of compensatory antioxidant mechanisms.

Chronic Addiction to Tramadol and Withdrawal Effect on the Spermatogenesis and Testicular Tissues in Adult Male Albino Rats

Pharmacology ◽  
2019 ◽  
Vol 103 (3-4) ◽  
pp. 202-211 ◽  
Author(s):  
Marwan Abdel-Latif Ibrahim ◽  
Alaa-Eldin Salah-Eldin
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Adult Male ◽  
Rna Extraction ◽  
B Cell Lymphoma ◽  
Experimental Period ◽  
Male Rats ◽  
Control Group ◽  
Albino Rats ◽  
Withdrawal Effect

Aim: The present study aimed to elucidate the effects of tramadol on the testicular functions of adult male rats due to the chronic usage of tramadol and the effect of its withdrawal. Method: Adult male albino rats were classified into the following 3 groups: (I) a control administered with normal saline and (II) tramadol-treated rats (40 mg/kg b.w. orally) for 21 successive days; and (III) like the rats in the second group but kept for 4 weeks after the last tramadol dose to study the effect of tramadol withdrawal. At the end of the experimental period, blood was collected and specimens from testis were taken for histopathological, biochemical, and molecular studies. A reverse transcription-polymerized chain reaction after RNA extraction from specimens was detected for the anti-apoptotic and pro-apoptotic genes in testicular tissues. Also, malondialdehyde (MDA) was measured in tissues homogenate and antioxidant enzymes activities were evaluated. Results: The results of this study demonstrated histological changes in testicular tissues in groups II and III compared to the control group, accompanied with increased apoptotic index and proved by increased B-cell lymphoma-2 (Bcl-2) associated-X-protein and caspase-3 expression, whereas anti-apoptotic Bcl-2 markedly decreased. Moreover, in tramadol-abused and -withdrawal groups, the MDA level increased, while the antioxidant enzymes activity decreased and revealed oxidative stress, indicating that tramadol is harmful at the cellular level and can induce apoptotic changes in testicular tissues. The withdrawal effect showed signs of improvement, but it did not return to normal levels. Conclusions: It could be concluded that the administration of tramadol causes abnormalities on testicular tissues associated with oxidative stress, which confirmed the risk of increased oxidative stress on testicular tissues due to tramadol abuse.

scholarly journals Induction Effect of Bisphenol A on Gene Expression Involving Hepatic Oxidative Stress in Rat

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Sohrab Kazemi ◽  
Seydeh Narges Mousavi ◽  
Fahimeh Aghapour ◽  
Boshra Rezaee ◽  
Farzin Sadeghi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Bisphenol A ◽  
Corn Oil ◽  
Rna Extraction ◽  
Control Group ◽  
Induction Effect ◽  
Hepatic Oxidative Stress ◽  
Body Weights ◽  
Male Wistar Rats

Background and Objective.Bisphenol A (BPA) is an abundantly used xenoestrogenic chemical which may cause various disorders in body. In the present study, we sought to investigate the effects of various doses of BPA on hepatic oxidative stress-related gene expression in rats.Methods.Male Wistar rats weighing 150–200 g were used in this study. Three doses of the BPA (5, 25, and 125 μg/kg) in corn oil were administered as gavage during 35 consecutive days. After the experiment, the rats were expired and the livers were removed and stored at −80°C freezer for RNA extraction.Findings.The Real Time PCR showed increased expression of HO-1 in the rats receiving BPA doses compared to the control group. This effect was dose-dependent and higher at doses of 25 and 125 μg/kg than 5 μg/kg of body weight (p<0.05). It was also demonstrated that various doses BPA can increase GADD45B gene expression compared to control group. That expression was significantly dominant in the lowest dose (5 μg/kg) of the BPA (p<0.05). The final body weights (168.0±10.0 gr) in the treatment group [BPA (125 μg/kg)] showed a significant decrease compared to control group (191.60±6.50 gr).Conclusion.These findings demonstrate that BPA generated ROS and increased the antioxidant gene expression that causes hepatotoxicity.

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